Cytokines in the muscle tissue of idiopathic inflammatory myopathies: implications for immunopathogenesis and therapy

Eur Cytokine Netw. 1999 Dec;10(4):471-8.


The inflammatory myopathies (IM), dermatomyositis (DM), polymyositis (PM) and idiopathic inclusion body myositis (IBM) are acquired immune-mediated myopathies. About their pathogenesis and etiology no definitive insights are available yet. Here we present a review of cytokine studies in IM. Combined with cellular immunohistochemical findings a model is presented describing a common mechanism of immune activation in IM. This model is based on a "hit" triggering local cytokine production with dominance of pro-inflammatory cytokines, like IFN-gamma and Th1-mediated activities. The altered Th1-Th2 balance necessitates detection of the anti-inflammatory arm of immune activation, which includes Th2-derived IL-4, IL-1, and Th3/Tr1 derived IL-10 and TGF-beta. Redirection of the ratio provides targets for novel immunotherapy by direct inhibition of the IFN-gamma-mediated Th1 response, stimulation of Th3/Tr1, or IL-4-secreting Th2-cells, negative feedback inhibition with IFN-beta and IFN-gamma and inactivation of MHC molecules.

Publication types

  • Review

MeSH terms

  • Cytokines / immunology*
  • Humans
  • Immunosuppressive Agents / therapeutic use
  • Immunotherapy
  • Lymphocyte Activation / immunology
  • Models, Immunological
  • Muscle, Skeletal / immunology*
  • Muscle, Skeletal / pathology*
  • Myositis / immunology*
  • Myositis / pathology
  • Myositis / therapy


  • Cytokines
  • Immunosuppressive Agents